Understanding why “absence of evidence is not evidence of absence”BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g4751 (Published 01 August 2014) Cite this as: BMJ 2014;349:g4751
- Philip Sedgwick, reader in medical statistics and medical education1
- 1Institute for Medical and Biomedical Education, St George’s, University of London, London, UK
Researchers investigated the effects of a low glycaemic index diet in pregnancy on maternal and neonatal morbidity in a group of women at risk of fetal macrosomia (large for gestational age infants). A randomised controlled superiority trial was performed. The intervention consisted of a low glycaemic index diet from early pregnancy. The control treatment was no dietary intervention. Participants were women without diabetes, all in their second pregnancy, who had previously delivered an infant weighing greater than 4000 g. In total, 800 women were recruited and randomised to the intervention (n=394) and control treatment (n=406).1
The primary outcome was birth weight and the secondary outcome gestational weight gain. The mean birth weight for the intervention group was greater than for the control group, although the difference was not significant (4034 (SD 510) v 4006 g (497); mean difference 28.6 g, 95% confidence interval −45.6 to 102.8; P=0.449). Mean gestational weight gain was significantly less for the intervention arm (12.2 v 13.7 kg; mean difference −1.3 kg, −2.4 to −0.2; P=0.01). The researchers concluded that a low glycaemic index diet in pregnancy did not significantly reduce birth weight for large for gestational age infants, but it did have a significant effect on reducing gestational weight gain for women at risk of fetal macrosomia.
Which of the following statements, if any, are true?
a) In the population, it can be inferred that no difference exists between the low glycaemic index diet and the control treatment in mean birth weight